The Study Of The Glial Function With The Infection Of Different Rabies Virus

Rabies is a kind of high mortality-rate disease,caused by rabies virus(RABV)and induces neuroinflammation in humans and animals.Rabies virus has a high degree of neurotropism,and the current case of rabies is mainly caused by dog's bites.Rabies virus will not immediately spread at the first stage of infection,but replicate in the muscle tissue around the wound.Then it will enter the peripheral nervous system and transport via the neurons reverse axon.When reaching to the dorsal root ganglia,the viruses will start to proliferate,and then invade the central nervous system(CNS)and finally they begin to unscrupulously centrifugally spread.The neuron infection in CNS is fatal,however,the mechanism of viral escaping for immune surveillance in CNS is not clear.CNS contains several cell types,including neurons and glial cells,in which microglia is the immune cell and major phagocyte,monitoring the surrounding microenvironment,and astrocytes spread widely in the mammalian brain as supportive cells.Therefore,we focus on glial cells to study the mechanism of virus immune escape in CNS.The primary mixed glial cells were infected with 0.01 MOI of lab-adapted virus B2 C,wild strain AH08 or SX15,and the growth curve of virus was determined.The colocalization of different virus and lysosome was monitored.The influence of different viruses on microglial activation and differentiation was detected.The results showed that copy number of lab-adapted virus increased in the beginning and then decreased,while copy number of wild virus didn't increase.The lab-adapted virus could co-localized with lysosome but the wild virus could not.The lab-adapted B2 C significantly activated microglial cells and stimulated microglia to differentiate into inflammatory M1-type and the wild strains up-regulated the expression of CD172?,CD200 R and CX3CR1,which initiated the interaction of microglia and neuron.In conclusion,rabies virus escaped the surveillance of neuroimmunity may partially through the suppression of glial activation.Theoretically,our study revealed a possible mechanism of rabies immune evasion,and provided a foundation on rabies control and prevention.